despoder
face farmin shortcel
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Originally, this was supposed to be a reply to the one retard el bastardido or some shit's post, as it decided to pop back up on my recommended, but I was putting in too much effort, so it gets its own post. The mechanisms here are very oversimplified, and I highly recommend reading into it further if you want to pursue this theory. DYOR, I am not a spoon.
To approach the idea of lightening eyes, you need to understand the basic anatomy of the iris. The iris doesn't function like the skin. The mechanics behind iris pigmentation differ from the epidermis, which is constantly renewing itself, so stuff like tyrosinase inhibitors doesn't work on it, while it will on skin. Your melanocytes in your iris do not turn over. Inhibiting tyrosinase doesn't remove healthy melanocytes, and they will persist. They will continue to form melanosomes and continue to exhibit tyrosinase activity.
Tyrosinase is also pretty fucking important for ganglion cells wiring back into the brain. Inhibiting it will fuck your vision. But as I said, melanocytes are fixed anyway, and inhibiting it won't reduce the number of melanocytes or the amount of melanin, just rate-limit the production of the latter.
Your melanocytes deposit and physically anchor within the first 3 years ish of your life. To "lighten" your eyes, you literally have to remove the melanocytes by force (usually done by laser, trauma, or fucking cancer, among others) or get your immune system to do it.
Fortunately, we do have some agents that have been shown to work.
Levobunolol causes a localized Horner's syndrome-like effect, which prevents melanocytes from permanently producing melanin by stopping the parasympathetic nervous system. This differs from tyrosinase inhibition, as levobunolol binds to melanin quite effectively (but has to accumulate, which is why it has to be used for a while). Levobunolol effectively causes melanocytes to go dormant. It prevents new melanosomes from being produced. Without melanosomes being produced and maintained, macrophages remove melanocytes as they aren't seen as useful anymore. They are effectively dead space, and your body isn't fond of that. Your immune system does its job.
On the other hand, Moxifloxin literally lyses the melanocytes (gross oversimplification). However, moxi can also damage the back layer of the iris, which can lead to pretty crazy side effects like vision issues, permanent photophobia, and pupils that basically become fixed and unable to react to light. This isn't simply a chemical alternative to lasers, as lasers only target the upper layer, but again, shit can happen with that too. I don't like this pathway personally.
Ideally, if you want to lighten your eyes, pharmacologically take the levobunolol route and be consistent with it for years. It is relatively safe for long-term use, as cancer patients or people with ocular hypertension regularly use it to reduce ocular pressure. Theoretically, you could also use a drug that increases macrophage activity to clear those dormant melanocytes caused by levobunolol administration. Inhibiting ROCK seems to be the most likely idea and, conveniently enough, netarsudil, another glaucoma med, comes as an eye drop and theoretically could work. Netarsudil, however, has been shown to cause corneal verticillata. Be careful with it. Statins also seem to increase this filtration and ease for macrophages to clear stuff out.
Or just put aside a fund and get that laser treatment.
Feel free to fact-check. I'm 90% sure this should be gtg. If y'all wanna be my guinea pigs, go for it.
To approach the idea of lightening eyes, you need to understand the basic anatomy of the iris. The iris doesn't function like the skin. The mechanics behind iris pigmentation differ from the epidermis, which is constantly renewing itself, so stuff like tyrosinase inhibitors doesn't work on it, while it will on skin. Your melanocytes in your iris do not turn over. Inhibiting tyrosinase doesn't remove healthy melanocytes, and they will persist. They will continue to form melanosomes and continue to exhibit tyrosinase activity.
Tyrosinase is also pretty fucking important for ganglion cells wiring back into the brain. Inhibiting it will fuck your vision. But as I said, melanocytes are fixed anyway, and inhibiting it won't reduce the number of melanocytes or the amount of melanin, just rate-limit the production of the latter.
Fyi, the tyrosinase inhibitor pathway was attempted with a better fucking drug than kojic acid, ampt, to treat pigmentation caused by latanoprost. It failed and was abandoned. The drug was trialed literally for eye depigmentation; if this shit worked, we would see this everywhere, even if never fully pushed for development. AAS like MENT are still used, even if it was abandoned. If you think a drug needs to be clinically used/in development to be effective, you're exhibiting the simple appeal to authority fallacy. Drugs are made and dropped all the time.
Your melanocytes deposit and physically anchor within the first 3 years ish of your life. To "lighten" your eyes, you literally have to remove the melanocytes by force (usually done by laser, trauma, or fucking cancer, among others) or get your immune system to do it.
Fortunately, we do have some agents that have been shown to work.
Levobunolol causes a localized Horner's syndrome-like effect, which prevents melanocytes from permanently producing melanin by stopping the parasympathetic nervous system. This differs from tyrosinase inhibition, as levobunolol binds to melanin quite effectively (but has to accumulate, which is why it has to be used for a while). Levobunolol effectively causes melanocytes to go dormant. It prevents new melanosomes from being produced. Without melanosomes being produced and maintained, macrophages remove melanocytes as they aren't seen as useful anymore. They are effectively dead space, and your body isn't fond of that. Your immune system does its job.
On the other hand, Moxifloxin literally lyses the melanocytes (gross oversimplification). However, moxi can also damage the back layer of the iris, which can lead to pretty crazy side effects like vision issues, permanent photophobia, and pupils that basically become fixed and unable to react to light. This isn't simply a chemical alternative to lasers, as lasers only target the upper layer, but again, shit can happen with that too. I don't like this pathway personally.
Ideally, if you want to lighten your eyes, pharmacologically take the levobunolol route and be consistent with it for years. It is relatively safe for long-term use, as cancer patients or people with ocular hypertension regularly use it to reduce ocular pressure. Theoretically, you could also use a drug that increases macrophage activity to clear those dormant melanocytes caused by levobunolol administration. Inhibiting ROCK seems to be the most likely idea and, conveniently enough, netarsudil, another glaucoma med, comes as an eye drop and theoretically could work. Netarsudil, however, has been shown to cause corneal verticillata. Be careful with it. Statins also seem to increase this filtration and ease for macrophages to clear stuff out.
Or just put aside a fund and get that laser treatment.
Feel free to fact-check. I'm 90% sure this should be gtg. If y'all wanna be my guinea pigs, go for it.
